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105 Cards in this Set
- Front
- Back
HIPAA
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Health Insurance Portability & Accountability Act of 1996
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HIPAA goals
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1) protects PT's info
2) provides for appropriate uses |
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3 acceptable uses for PHI
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1) treatment
2) payment 3) operations |
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Minimum Necessary Rule
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least info possible to complete task
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golden rule
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everything seen and heard should be left at the scene
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golden rule does not apply to
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-PT treatment
-billing -quality assurance -critical incident situation debriefing |
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Dispatch and response acceptable uses
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-sharing info with other units
-talking to family members -info to and from bystanders -ok to transmit PHI to hospital -ok to transfer PCR |
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After the call acceptable uses
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-discussions with crew
-QA/CISD |
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Law Enforcement Disclosures
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-we are PT advocates
-drinking - no -health stuff ok |
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Notice of Privacy Practices
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get signature for non-emergent patients
-emergent not req'd |
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Mass Casualty Incidents
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ok to disclose PHI
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PT acess
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Direct PT to admin
-PT may request ammendment of info, we are not obligated to change |
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Safeguarding PT info (3 catagories)
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1) Written - locked cabinet role based
2) Verbal - use most secure method to tansmit, be aware of voice volume 3) Electronic - password protection fax with cover sheet |
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victim of a crime
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tell law enforcement
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Breakdown of water types in the body
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60% water weight
Plasma - 4% Interstitial Fluid - 16% Intracellular Fluid - 40% |
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What happens as the body begins to sweat?
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liquid leaves the skin via the ICF/ECF, fluid leaves the blood stream to replace
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Fluids IV (3 types)
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Hypotonic - low concentrate levels - pure water
Hypertonic - high concentrate levels - D50 (dextrose) Isotonic - same level of stuff - 0.9% NaCl |
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How does R sided CHF affect blood pressure?
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increased venous pressure (up from 2-10)
causes edema |
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normal arterial and venule pressures
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arteriole - 120
venule - 2-10 |
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Edema pooling locations
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ambulatory - legs and feet
non-ambulatory - butt |
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pH
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Potential for Hydrogen
ACID 1 ------------------------14 BASE acids donate hydrogen ions, bases receive |
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Normal pH operating range
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7.35-7.45
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3 Balancing Methods
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1) Renal = (Days) Effective but slow
-recapture Bicarb, secrete H+ 2) Respiratory = (minutes) middle effectiveness 3) Carbonic Acid = (instant) not very effective -ICF |
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Carbonic Acid
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H2CO3
-temporary portal to either side of equation |
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Carbonic Acid Full Equation
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H2O + CO2 <-> H2CO3 <-> H + HCO3
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4 IMBA's
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OD with bicarb = metabolic alkalosis
Pooping = metabolic acidosis Not Breathing = respiratory acidosis Hyperventilation = respiratory alkalosis |
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Ex. Cyanosis with clear lungs ?
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pulmonary embolism, no blood gets to the lungs to profuse
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Normal Operating Range for PO2 and PCO2 in body
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PO2 = 80-100 Normal
PCO2 = 35-40 Normal |
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Is P02 affected in metabolic acidosis or alkalosis?
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No
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PH 7.2
PO2 40 PCO2 80 RR 4 |
Respiratory Acidosis,
RR is extremely slow, PO2 is bad |
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PH 7.2
PO2 40 PCO2 80 RR 36 |
Respiratory Acidosis
Ineffective Respiration's due to CHF |
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PH 7.7
PO2 100 PCO2 80 RR 8 |
Metabolic Alkalosis
No hyperventilation, RR is trying to compensate |
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PH 7.8
PO2 90 CO2 20 RR 8 |
Metabolic Alkalosis
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PH 7.33
PO2 80 PCO2 60 RR 30 |
Metabolic Acidosis
O2 is fine, RR is trying to compensate |
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PH 7.8
PO2 100 PCO2 30 RR 36 |
Respiratory Alkalosis
PO2 is fine RR is way too high |
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PH 7.8
PO2 100 PCO2 20 RR 8 |
Metabolic Alkalosis
PO2 is fine, RR is low |
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PH 7.2
PO2 40 PCO2 80 RR 8 |
Respiratory Acidosis
PO2 is bad, RR is slow. |
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Types of Shock (5)
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1) Hypovolemic - volume is too low
-dehydration slow -hemorrhagic - fast 2) Cardiogenic - Heart damage due to tissue death ) 40% heart DMG is fatal 3) Nuerogenic Shock - loss of sympathetic motor tone -arterioles begin to dilate 4) Anaphylactic shock - severe allergic reaction -fluid moves to tissue, BP bottoms out, airways constrict 5) Septic Shock - systemic bacterial infection -fluid is fine, cells can't unload toxins properly |
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Baroreceptors Location and function
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located in arch of aorta, R atria, carotid arteries
react to pressure change, satisfied (BP ok), unsatisfied (BP low) -signal to heart to increase rate and strength, increase vasoconstriction |
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peripheral vascular reistance
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affects the pressure of the blood by constricting
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catecholomines
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hormones that stimulate A1, A2, B1, B2
Epinephrine |
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A/B receptors location
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Alpha 1 = arterioless
Beta 1 = heart Beta 2 = lungs (dilate bronchioles) |
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Vascular properties
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arteries - very elastic
arterioles - muscles change in size, tight = high BP Capillaries - no change in size |
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4 Basic Types of tissue
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1) Epithelial tissue
2) Connective tissue 3) Muscle tissue 4) Nervous tissue |
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Who has more water content babies or old people? male or female? fat or skinny?
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Males, Babies, and Skinny people have a higher water content
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Mediated Transport Mechanisms
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Required to move large water soluble molecules or electrically charged molecules across cell membranes,
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Active Transport vs Facilitated Diffusion
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Active transport moves molecules against a concentration gradient, lower to higher
Facilitated Diffusion is passive and molecules go from areas of high to low concentration. with the gradient. no energy required |
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arterioles & metarterioles components
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arterioles > Metarterioles > Capillaries
either true capillaries or thoroughfare channels which bypass the capillaries and connect arterioles and venules Precapillary Sphincters control blood flow through the capillaries |
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AV shunts
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non-nutritional/shunt flow, help regulate body temp, found in sole of the foot, palm of the hand, phalanges and nail bed
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Regulation of blood vessels
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both vasoconstrictor and vasodilator, sympathetic system is the most important.
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normal circulation characteristics
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arterioles are open, AV shunts closed, 20% capillaries open at a given time
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Diffusion across the capillary wall
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nutrients diffuse across the capillary wall into the interstitial fluid to enter the cells.
Metabolic end products diffuse across cell membrane into the extracellular fluid |
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Starling's Hypothesis
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Net Filtration = Forces Favoring Filtration - Forces opposing filtration
At arteriole end - filtration +HIGH Blood pressure +LOW negative interstitial pressure -LOW Blood colloid osmotic pressure (low because lots of fluid still in) Venous End - inward forces -HIGH Blood Colloid osmotic pressure (low fluids in vessel, so high particle concentration) +LOW blood pressure +LOW negative interstitial pressure |
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membrane permeability
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if permiability changes, particles may escape from the lumen into the interstitial space, lowering the blood oncontic pressure. Edema results
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4 Factors causing edema
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1) Increase in the hydrostatic pressure
2) Decreased Plasma Oncotic Pressure 3) Increased Capillary Permeability 4) Lymphatic obstruction |
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localized vs generalized edema
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localized is limited to an injury site or an organ system (sprained ankle)
generalized is widespread swelling due to chronic conditions including heart disease, kidney, and liver disease |
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ADH
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antidiuretic hormone - helps to regulate water balance
-released with high plasma osmolality or a decrease in circulating blood volume -puts aquaporins in the DCT of nephrons reclaims most of the water in urine |
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Normal ratio of carbonic acid to bicarbonate
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20 : 1 at pH of 7.4
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what determines our respiratory rate?
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the pH
hemoglobin binds with carbon dioxide and hydrogen ions. at the lungs the hydrogen ions combine with bicarb forming Carbonic acid which becomes CO2 and H2O, which is exhaled |
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Renal Buffering Components (3)
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1) recovery of bicarb
2) secretion of hydrogen ions into urine 3) excretion of ammonium ions, which carry a hydrogen ion with it |
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Respiratory Acidosis symptoms
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-respiratory depression
-respiratory arrest -cardiac arrest -neuromuscular impairment -medications (sedatives, hypnotics) -chest wall injury -pulmonary disorders |
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4 Main causes of Metabolic Acidosis
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1) Lactic Acidosis
-the body switches from aerobic to anaerobic respiration, creating lactic acid which releases hydrogen ions 2) Diabetic Ketoacidosis -pt fails to take enough insulin, fatty acids are metabolized producing ketone bodies and releasing hydrogen ions 3) Acidosis by renal failure -kidneys reclaim bicarb and release Hydrogen if working properly 4) Acidosis caused by ingestion of Toxins |
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Respiratory Alkalosis can be caused by...
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hyperventilation
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Mixed acid-base disturbances are commonly seen in pt's with what condition?
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SHOCK
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5 most signifcant adaptive changes in cells
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1) atrophy - decrease in size
2) hypertrophy - increase in size 3) hyperplasia - excessive increase in the number of cells (in a row) 4) metaplasia - a change from one cell type to another that is better able to tolerate adverse conditions (not normal for that cell type) 5) dysplasia - abnormal changes in mature cells |
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Hypoxic injury
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cell damage
lack of oxygen due to athersclerosis or thrombois leads to infarction or cell death |
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Chemical Injury
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cell damage
toxins or chems may affect cell membrane permiability, or disrupt cellular metabolism |
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Infectious Injury
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cell damage
bacteria create exotoxins, they carry the genetic material to make the toxin -also activate the inflammatory process virusus - genetic material encapsulated, require a host to replicate |
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Immunological & inflammatory injury
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cell damage
cells are damaged by the cells causing inflammatory responses, as well as complement If the Na/K pump breaks, the cell may swell and rupture |
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Genetic Factors
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cell damage
inherited abnormal cell characteristics |
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Nutritional Imbalances
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cell damage
rickets, scurvey, obesity etc |
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physical agents
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cell damage
-temperature extremes, atmospheric pressure, radiation, illumination, mechanical stress |
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Cellular manifestations of injury (3)
what happens when cells are injured? |
1) cellular swelling
resulting from membrane changes, K out Na in. Water follows Na, increased swelling 2) Fatty Change -enzyme systems that metabolize fat are impaired and overwhelmed. lipids accumulate inside the cell 3) system manifestations -fever, malaise, loss of well being, change in appetite, altered heart rate and rise in WBC |
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shock
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decreased cardiac output, hypoprofusion
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cardiac output
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depends on several factors, including strength of contraction, rate of contraction and he amount of blood returning through the veins.
SV X HR |
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chemoreceptor reflexes
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compensatory mechanism
found in the carotid and aortic bodies, activated by PO2 or pH decrease, vasomotor center of the medulla stimulated, rate and depth of ventilation increased can also stimulate vasomotor to enhance PVR |
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central nervous system ischemic response
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compensatory mechanism
blood flow to the vasomotor center of the medulla. nuerons in the vasomotor center become excited, raising the arterial blood pressure does not activate until the blood pressure falls below 50mmHg 10 minute duration |
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Hormonal mechanisms that increase BP
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compensatory
1) renin-angiotensin-aldosterone & vasopressin (renin released by kidneys, becomes angiotensin 2 in lungs = vasoconstriction) 2) aredenal medulla secretes epi and noreppie 3) vasopressin (ADH) |
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Splenic discharge of blood
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some of the blood that circulates through the spleen is stored in an area called the venous sinususes. (300ml) expelled during hypotension
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reabsorption of tissue fluids
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lowered BP means less hydrostatic pressure, less fluid moving into the capillaries
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MODS
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multiple organ dysfunction syndrome
triggered by the body's inflammatory response consists of 3 systems -complement (further damages epithelial membrane) -coagulation -kallikrein (vasodilation) Hyperdynamic circulation > increase demands on the heart > depletion of O2 and fuel > decreased O2 to cells/hypermetabolism/myocardial depression > multiple organ failure > tissue hypoxia |
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Impairment of cellular metabolism
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-anerobic production of ATP inefficient, releases lactic acid and hydrogen ions
-ions begin to accumulate, causing vasodilation -post capillary sphincters resistant, so capillaries more permeable, fluid enters ECF -inefficent ATP production hinders Na/K pump, causing decreased membrane potential and eventually cell damage |
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3 lines of body defense
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1) external barriers, skin and mucous membranes
2) inflamatory response 3) immune response |
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inflammatory response 3 stages
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1) cellular response to injury
-damage to cell causes membrane permiability, organelle permiabiity, hydrolytic enzymes release and the cell undergoes apoptosis 2) Vascular response to injury -increased blood flow to injured area causes edema luekocytes begin to gather along the vascular endothelium as a result of chemical attractants. 3) phagocytosis -luekocytes engulf, digest, and destroy pathogens, eventually lysis occurs and pus is created |
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MAST cells
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cytoplasm is filled with granules containing vasoactive amines and chemotactic factors
stimulated by trauma, or physical injury, or chemical agents (bee sting) cause inflammation |
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local vs system responses to acute inflammation
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local
-vascular changes (vasodilation) -formation of pus systemic -fever -leukocytosis -increase in circulating plasma proteins |
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response to chronic inflammation
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inflammation that lasts 2 weeks or longer
-connective tissue fibers and new blood vessels -large area = scar tissue forms |
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Acquired immunity
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exposure to a specific antigenic agent or pathogen
-exposure can be in the form of a vaccination |
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Humoral Immunity VS Cell mediated Immunity
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Both considered acquired immunity
humoral immunity -production of antibodies that combine and kill the invader cell mediated immunity -formation of a group of lymphocytes that attack and destroy foreign material |
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antigen vs immunogen and components of
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antigen is a substance that reacts with preformed components of the immune system
immunogen is a specific type of antigen that can bring about or induce the formation of antibodies. they must be -sufficiently foreign to the host -sufficiently large -sufficiently complex -present in sufficient amounts |
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creation of B and T cells and differences between
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phagocytes digest foreign material and antigenic material appears on their surface.
-some mature into B Plasma cells that produce antibodies -some mature into sensitized T lymphocytes that directly hunt and kill the antigen |
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Universal Donor vs. Recipient and Rh factor
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Universal donor is O
Universal Recipient is AB A has anti B antibodies B has anti A antibodies O has both antibodies AB has none Rh factor is another protein 85% of people have it. |
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allergy, autoimmunity and isoimmunity
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allergy - refers to an exaggerated immune response by environmental allergens (most common, least life threatening)
autoimmunity - immune response against the host's own cells isoimmunity - immune response directed against beneficial foreign tissues (blood transfusion) |
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IgE reactions
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accounts for less then 1% of the AB in normal serum
-responsible for immediate (type I) hypersensitivity reactions. -bound to mast cell or basophils, cause these cells to release chemical mediators when antigens bind |
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IgG
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70-73% of the antibodies in serum
most abundant in blood, but found in lymph, cerebrospinal fluid, synovial, pertioneal fluid, breast milk -secondary immune response -crosses placenta |
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IgM
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5-10%
-trigger increased production of IgG in acute infections and complement fixation required for an effective AB response |
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IgA
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15%
-blood, tears, saliva, RT, stomach, organs -combines with a protein in mucosa that defends body surfaces agains invading microorganisms |
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IgD
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less then 1%
unknown function |
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Acquired Deficiencies 5 groups
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Much more common then congenital forms
1) nutritional deficiencies 2) Iatrogenic deficiencies (caused by some form of medical treatment) 3) deficiencies caused by trauma (bacterial infections, burns) 4) deficiencies caused by stress (depressed immune function) 5) Acquired Immunodeficiency Syndrome (AIDS) |
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psychoneuroimmunology
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study of the three way interaction of the emotional state, the central nervous system, and the body's defense against external infection and abnormal cell division
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stress response
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activates the sympathetic nervous system
catecholomines (eppie/noreppie, and dopamine) released into the blood stream hypothalamus stimulates the pituitary gland to release ADH, prolactin, growth hormone, and adrenocorticotropic hormone (ACTH) ACTH stimulates the cortex of the adrenal gland to release cortisol |
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cortisol effects what?
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stimulation of gluconeogensis, by reducing glucose utilization
slows down immune cell activity, helps prevent damage |
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factors that cause disease
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genetics, environment, age and gender
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analyzing the risk of disease
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incidence/prevalence/mortality rate
causal risk factors/noncausal risk factors |
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familial disease tendency
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due to genetic factors or shared environmental factors
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